DIAG, a laboratory information management system developed for regional animal disease diagnostic laboratories in Indonesia.

The DIAG Laboratory Information Management System is a micro-computerised program designed for the use of regional and national animal disease diagnostic laboratories in Indonesia. It facilitates the day to day management of diagnostic data by monitoring the progress and turn round times of samples sent to laboratory sections and by printing outputs detailing the tests undertaken and results obtained. Notifiable disease reports are generated routinely as part of a national disease surveillance programme. Detailed analyses of specific diagnoses allow investigations of diseases over location and time. The database is easily accessed to allow additional analyses. Data entry is facilitated through the use of entry screens which reduce associated errors. The system is flexible and can readily be adapted to meet the demands of different countries, veterinary services and types of laboratory.

Effects of N-nitrosopyrrolidine, nitrite and pyrrolidine on tumour development in mice as related to ingestion of cured meat.

The incidence of tumours in mice fed a standard chow diet and given either N-nitrosopyrrolidine (NPyr), nitrite (NO(2)) or nitrite plus pyrrolidine (NO(2) + Pyr) in the drinking water for 12 months at 100mg, 1 g and 1 g plus 100mg/litre, respectively, was compared with that for a control group (C) receiving no additives. Differences between groups in weight gain and feed consumption were not significant. Group 3 (NO(2)) drank less water (P < 0·05) than those in groups 1 (C) and 2 (NPyr). Water intake of mice in group 4 (NO(2) + Pyr) did not differ from that of any of the other three groups. Survival rates were: 94% (C), 80% (NPyr), 92% (NO(2)) and 83% (NO(2) + Pyr); but the differences were not statistically significant. Gross examination upon autopsy revealed that the incidence of all tumours in group 2 (NPyr) was 10- to 20-fold higher than that in any other group. Histological examination confirmed that NPyr induced more (P < 0.05) malignant tumours in liver and lungs with any other treatment; otherwise there were no significant differences. Results indicated that NO(2) + Pyr (nitrite plus a secondary amine) did not increase the frequency of carcinogenic tumours in mice.

Polybrominated biphenyl toxicosis in rats fed an iodine-deficient, iodine-adequate, or iodine-excess diet.

Young male Sprague-Dawley rats were fed 0, 1, 10, or 100 ppm of polybrominated biphenyls (PBB) in iodine-deficient, iodine-adequate (0.2 ppm), or iodine-excess (1000 ppm) diets. Six rats in each of the 12 groups were killed at 30 days and the remaining six in each group at 60 days. Growth rates were similar in all rats fed diets containing 0, 1, or 10 ppm PBB but were slower from 30 to 60 days in rats given 100 ppm PBB. Results of routine hematologic examinations and urinalyses were essentially normal. Although liver weights were substantially increased by PBB, the smallest increases were in rats fed an iodine-deficient diet. Thyroid weights were increased by iodine deficiency and by 10 and 100 ppm PBB. Electropherograms of serum proteins, serum lipoproteins, and LDH isozymes at 60 days from rats given PBB indicated hepatic alterations, but changes were least dramatic in rats fed an iodine-deficient diet plus PBB and most severe in rats fed iodine-excess diets plus PBB. Hepatic lesions were basically similar to those previously described except that bile duct proliferation was seen at 60 days only in rats fed an iodine-deficient diet and 100 ppm PBB. Histologic changes in thyroid glands were associated with iodine deficiency and with PBB. The iodine-excess diet plus 100 ppm PBB induced squamous metaplasia of respiratory bronchiolar epithelium. These results indicate interrelationships between PBB and iodine which may affect the toxicosis caused by PBB.